Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The major risk factor associated with the appearance of adverse cardiovascular events and outcome attributable to cardiovascular disease is left ventricular hypertrophy (LVH). Why this should be so resides not in the increase in myocardial mass per se, but in the disruption of myocardial structure. An abnormal accumulation of fibrillar collagen within the adventitia of intramyocardial coronary arteries and neighboring interstitial spaces represents such a distortion in structure. Furthermore, this fibrosis disrupts the electrical and mechanical behavior of the hypertrophied myocardium. Mechanisms responsible for fibrillar collagen accumulation have been examined in intact animals and cultured cardiac fibroblasts. In vivo studies indicate that myocardial fibrosis is associated with the presence of chronic mineralocorticoid excess, relative to sodium intake and excretion, not hemodynamic workload. Accordingly, fibrosis can appear in both the hypertensive, hypertrophied and nonhypertensive, nonhypertrophied ventricles. In both primary and secondary hyperaldosteronism it was possible to prevent myocardial fibrosis with an aldosterone receptor antagonist, while in unilateral renal ischemia angiotensin converting enzyme (ACE) inhibition was similarly cardioprotective. A regression in fibrous tissue and normalization of diastolic stiffness has also been possible using ACE inhibition, bringing forward the concept of cardioreparation and the notion that heart failure due to fibrosis may be reversible. In vitro studies indicate that effector hormones of the renin-angiotensin-aldosterone system stimulate fibroblast collagen synthesis. Aldosterone, in pathophysiologic concentrations, and angiotensin II, in much larger concentrations, each enhance collagen synthesis without altering the mitogenic potential of these cells. Thus, elevations in circulating aldosterone and angiotensin II, relative to sodium intake, have the potential to not only alter sodium homeostasis and vascular tonicity, but also the structure of cardiovascular tissue. Thus, myocardial fibrosis represents a structural basis for pathologic hypertrophy and ultimately accounts for the appearance of adverse cardiovascular events and outcomes.
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PMID:Pathologic hypertrophy with fibrosis: the structural basis for myocardial failure. 136 63

A retrospective investigation was undertaken in which the rate of decline of residual renal function (RRF), estimated from creatinine clearance, was compared in 55 continuous ambulatory peritoneal dialysis (CAPD) and 57 hemodialysis (HD) patients for whom a minimum of four (mean of 7.6) well-spaced historic measurements of residual clearance were available. Because of the intrinsic variability that attends such data, specialized nonlinear, growth curve statistical methods were employed. Residual function was found to decline exponentially after the onset of therapy in both cohorts. The rate of decline in the HD group was twice that of the CAPD group (5.8% +/- 0.4% per month for HD vs 2.9% +/- 0.3% per month for CAPD; difference significant at p less than 0.0001). This difference remained highly significant (p less than 0.01) when corrected for other potential risk factors such as age, gender, hypertensive status, and use of angiotensin converting enzyme inhibitors in patients with diabetic or other forms of glomerular nephropathy. Differences between cohorts were not significant for patients with other diagnoses (p greater than 0.1) although the size of some of these subsets was very small. The physiologic mechanism for the more rapid fall-off of RRF on HD remains speculative, but could be related to renal ischemia secondary to intratreatment hypovolemia and/or to nephrotoxic effects of the inflammatory mediators of extracorporeal circulation.
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PMID:The influence of dialysis treatment modality on the decline of remaining renal function. 176 96

We evaluated 1525 consecutive patients who had undergone thoracic or thoracoabdominal aortic surgery to ascertain the factors associated with the development of acute renal failure. Complete data were available in 1233 patients who were treated recently, and these were analyzed. Acute renal failure, severe enough to require dialysis, developed in 5.5% of this group (68/1233): 2.3% and 7%, respectively, for descending (9/391) and thoracoabdominal repairs (59/842). Of interest, on multivariate analysis, both renal artery endarterectomy for occlusive disease (p = 0.0006) and chronic dissection (p = 0.03) were associated with significantly less acute renal failure. On multivariate analysis, the significant independent predictors (p less than 0.05) of acute renal failure were preexistent renal dysfunction, evidence of diffuse atherosclerosis, the use of the pump bypass, and markers of hemodynamic instability. Contrary to earlier reports based on a smaller number of patients, we found that neither the use of pump bypass (7% acute renal failure), atriorenal bypass (8% acute renal failure), nor cold Ringer's lactate (3% acute renal failure) appeared to significantly avert the complication of acute renal failure. Indeed, pump bypass appeared to be deleterious (p = 0.0146) and perfusion with cold Ringer's lactate was not without risk. Furthermore, in a prospective evaluation of angiotensin converting enzyme blockers, we were unable to show that they afforded renal protection after transient renal ischemia. This study has clarified the clinical problems associated with acute renal failure and lays the foundation for future research.
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PMID:Appraisal of adjuncts to prevent acute renal failure after surgery on the thoracic or thoracoabdominal aorta. 277 85

Little attention has been paid to nephropathies and proteinuria in renovascular hypertension (RVH). Recently there has been a growing interest in the conditions induced by RVH. 10 cases of RVH were diagnosed by angiography and renin sampling from renal veins in the last 6 years in our hospital. The patients were all male and mean age was 64 +/- 8 (SD) years. Data were as follow: protein excretion was 3.8 +/- 2.2 g/day (> or = 3.5 g/day in 8 patients), sBP 202 +/- 24 mmHg, dBP 113 +/- 17 mmHg, serum renin concentration 64 +/- 45 pg/ml, and ipsilateral/contralateral renal vein renin ratio 3.3 +/- 1.0. RVH was treated by nephrectomy in 3 patients, percutaneous transluminal renal angioplasty (PTA) in 2, and angiotensin converting enzyme inhibitors (ACE-I) administration in 8. Biopsies were performed on contralateral kidney in 4 patients. Focal segmental glomerulosclerosis (FGS) was found in 3 patients, and nephrosclerosis in 1, whereas only nephrosclerosis was found in nephrectomized kidneys in all 3 patients. After nephrectomy, PTA and the treatment by ACE-I, not only blood pressure but also proteinuria was markedly reduced. These findings suggest that severe stenosis of the renal artery led to renal ischemia, which activated renin excretion, to cause glomerular hyperfiltration through vasoconstriction of the efferent arterioles in the contralateral kidney. FGS-like lesion thus induced appeared to have caused massive proteinuria.
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PMID:Renovascular hypertension may cause nephrotic range proteinuria and focal glomerulosclerosis in contralateral kidney. 935 55

Ischemic renal disease (IRD) is defined as a clinically important reduction in glomerular filtration rate or loss of renal parenchyma caused by hemodynamically significant renal artery stenosis. IRD is a common and often overlooked clinical entity that presents itself in the setting of extrarenal arteriosclerotic vascular disease in older individuals with azotemia. Eleven to 14% of end-stage renal disease (ESRD) cases are attributable to chronic IRD. A high percentage of patients entering ESRD programs are hypertensive. Many patients with a presumed diagnosis of hypertensive nephrosclerosis actually have undiagnosed ischemic nephropathy as the etiology of their ESRD. It is important for the clinician to identify IRD, because IRD is a potentially reversible cause of chronic renal failure in a hypertensive patient. Atherosclerotic renal artery disease is common among patients with coronary artery disease and aortic and peripheral vascular disease. Atherosclerotic renal artery disease is a progressive disorder, and its progression is associated with loss of renal mass and functioning. A decrease in glomerular filtration rate sufficient to cause an elevation of the serum creatinine concentration requires injury to both kidneys. Consequently, IRD can arise from one of two main clinical situations: bilateral hemodynamically significant renal artery stenosis leading to bilateral renal ischemia; and hemodynamically significant renal artery stenosis in a solitary functioning kidney, or in a kidney that is providing the majority of a patient's glomerular filtration. The primary reason for establishing the diagnosis of IRD is the hope that correction of a renal artery stenosis will lead to improvement of renal function, or a delay in progression to ESRD. There are six major clinical settings in which the clinician could suspect IRD: acute renal failure caused by the treatment of hypertension, especially with angiotensin converting enzyme inhibitors; progressive azotemia in a patient with known renovascular hypertension; acute pulmonary edema superimposed upon poorly controlled hypertension and renal failure; progressive azotemia in an elderly patient with refractory or severe hypertension; progressive azotemia in an elderly patient with evidence of atherosclerotic disease; and unexplained progressive azotemia in an elderly patient. Noninvasive testing modalities that have been used recently include the angiotensin converting enzyme inhibitor renal scan, duplex Doppler sonography, magnetic resonance angiography, and the spiral computed tomography. Treatment methods include percutaneous transluminal angioplasty, endovascular stenting, and surgical revascularization. The results of treatment for preservation of renal function have been encouraging, with stabilization or improvement in renal function observed in a significant proportion of cases.
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PMID:Ischemic renal disease: an emerging cause of chronic renal failure and end-stage renal disease. 943 40

The present study was designed to investigate the effect of captopril, a sulfhydryl (-SH) containing ACE inhibitor and lisinopril, a non-SH containing ACE inhibitor, on ischaemia-reperfusion-induced renal injury in rats and to study the involvement of the free radical scavenging property of captopril in its renoprotective effect. Bilateral renal artery occlusion was induced for 30 min followed by reperfusion for 24 h. Blood samples were taken from retro orbital sinus before surgery and at 24 h after reperfusion for blood urea and blood creatinine estimation. After completion of 24 h of renal reperfusion the carotid artery was cannulated and the mean arterial blood pressure (MABP) was recorded. The left kidney was used for histological examination. The right kidney was utilised for estimation of mitochondrial thiobarbituric acid reactive substances (TBARS). Renal ischaemia, followed by reperfusion, significantly increased blood urea nitrogen (BUN) and blood creatinine. However, creatinine clearance decreased markedly. Captopril administered before renal artery occlusion or immediately after reperfusion and lisinopril pre-treatment significantly attenuated the increase in BUN and blood creatinine. Creatinine clearance was markedly better in captopril-treated animals as compared to lisinopril-treated rats. Captopril significantly decreased the degree of tubular necrosis, haemorrhagic streaks and urinary casts. Lisinopril treatment decreased tubular necrosis and urinary casts but no marked effect on haemorrhagic streaks was noted. Administration of captopril before ischaemia or just after reperfusion significantly reduced the elevated concentration of mitochondrial TBARS but no such decrease was noted in lisinopril-treated rats. Based on these results it may be concluded that captopril and lisinopril markedly protected against ischaemia-reperfusion-induced renal injury and any additional renoprotective effect of captopril may be ascribed to its free radical scavenging properties.
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PMID:Effect of angiotensin converting enzyme inhibitors on ischaemia-reperfusion-induced renal injury in rats. 950 76

The renin-angiotensin system is initiate by numerous pathological situations which release the renal ischemia: heart failure, arterial hypertension, renal pathology with or without diabetes mellitus. Therapeutic possibilities in renin-angiotensin system control are offered by angiotensin-converting enzyme inhibitors, angiotensin II type-1 receptors antagonists, angiotensin converting enzyme inhibitors and neutral endopeptidase inhibitors and angiotensin II type 2 receptors agonists.
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PMID:[The renin-angiotensin system:implications, pathology, therapeutic possibilities, perspectives]. 1209 17

Over a period of six months, 55 patients out of 11,216 (0.49%) admitted to the hospital developed acute renal failure (ARF). The diagnosis of ARF was based on the usual criteria, a sudden rise in blood urea nitrogen and creatinine with or without oliguria. Patients age ranged between 15 and 81 years with a mean of 51.9 years. Renal ischemia (69%) and nephrotoxic drugs (16.3%) were the two main etiologic factors. Among the causes of ischemia, septic shock was the commonest (29%), followed by severe hypotension due to several causes such as hemorrhage, burns, severe diarrhea and cardiogenic shock (25.4%), and ACE inhibitors (10.9%). ARF was associated with an average of 15.8 days stay in hospital versus 5.1 days for the overall hospital admissions. Immediate management of hypotension by intravenous fluid replacement, vasopressor agents and the necessary surgical intervention was appropriately considered. Intravenous frusemide was used for oliguric patients. Intermittent hemodialysis was used in 18 patients and continuous venovenous hemofiltration in six patients. Twelve patients with ARF due to ischemia died, while there were no deaths in the nephrotoxic group (p < 0.05). The overall mortality was (21.8%), which had no correlation with patient age. All non-oliguric patients survived with the mortality being exclusively in the oliguric group.
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PMID:Acute renal failure: six months pilot study in qatar. 1840 4

Ischemic preconditioning has been first described by Murry and coworkers as the protection conferred to ischemic myocardium by preceding brief periods of sublethal ischemia separated by periods of reperfusion. Another phenomenon closely associated to IPC is hibernation and stunning. The hibernating myocardium refers to resting left ventricular dysfunction due to reduced coronary blood flow that can be partially or completely reversed by myocardial revascularization and/or by reducing myocardial oxygen demand. Similarly as for the myocardium, these effects are reproducible for other solid organs. Here we report a case of a renal transplant recipient with decompensated proximal transplant artery stenosis due to ACE inhibition resulting in acute renal failure. The transplant perfusion was strictly dependent on systemic arterial blood pressure leading to intermittent episodes of renal ischemia and reperfusion. Renal function was severely decreased (glomerular filtration rate approximately 8 ml/min) with the need of hemodialysis treatment over a period of 4 weeks after transplantation. After dilatation of the stenosis, the patient's renal function improved rapidly and achieved values better than ever before. Referring to the definition of hibernating myocardium, here we postulate a case of a hibernating kidney in context of ischemic preconditioning.
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PMID:A hibernating kidney - ischemic preconditioning in a renal transplant recipient with a proximal stenosis of the iliac artery. 1879 34

Scorpion venoms cause renal injury by the interaction of renal ischemia due to intense renal vasoconstriction and inflammatory reactions due to proinflammatory cytokines and mediators. Renal vasoconstriction is not only induced by catecholamine storm but also by angiotensin II and the direct action of venom on vascular ion channels. Increased aldosterone also contributes to hypertension. Blocking of renal tubular K channels decreases renal K excretion and increases serum K level which increases aldosterone release. Hyperaldosteronism increases K excretion mostly through ROMK2 and ROMK3 unblocked by the venom. The presence of angiotensin converting enzyme inhibitor in some scorpion species can increase serum K. Therefore, there are both K increasing and K decreasing effects in renal K excretion. Serum K in scorpionism is the net result of the two opposing effects. Hyperkalemia is therefore inconsistent.
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PMID:Scorpion venoms, kidney and potassium. 2383 19


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